中西医结合辨治慢性肾小球肾炎临床观察

用中西医结合辨治慢性肾小球肾炎的临床观察，初步证实该“益黄汤”并适当选用西药抗炎、调整酸碱平衡等方法达到具有消肿、增加尿量、减少尿蛋白、改善贫血、降低血尿素氮、肌酐浓度等病况，均有一定的临床疗效．     

Protein Subcellular Localization Prediction and Genomic Polymorphism Analysis of the SARS Coronavirus

Introduction In March 2003, a novel coronavirus (CoV) was dis-covered in association with the outbreak of severe acute respiratory syndrome (SARS)[1-3]. The complete genome sequence of several SARS-CoV isolates was soon determined and characterized[4,5]. Comparison of variant SARS-CoV genome sequences has identified certain genetic signatures that can be used to trace sources of infection[6]. Vaccines are now being devel-oped and molecular modeling has suggested that modi-fied rhinovir…     

基于体动射频信号的睡眠分期

为了减轻传统接触式睡眠生理监测系统对人体造成的负担,设计了一种基于微波技术的非接触式睡眠生理信号采集与分析系统,提出一种基于体动射频信号的睡眠分期识别算法.通过小波变换对射频运动传感器(RFMS)采集的体动信号进行预处理,再计算出体动信号的能量值,最后通过判别式处理和阈值法实现了睡眠分期:醒觉期、浅睡期、中睡期、深睡期.实验采集分析了8个实验者为期46天的睡眠生理信号,同时同步采集视频信息、TANITA水床睡眠信息、接触式呼吸脉搏信号.与视频结果比较发现醒觉期正确率达到90%;与TANITA水床睡眠结果相比,本系统的结果与其吻合程度达到70%;与不同睡眠状态下呼吸率、心率的变化相比,本系统的结果吻合度达到80%.     

围绝经期综合征舌苔脱落细胞凋亡调控蛋白与肝郁病理的相关性

通过研究围绝经期综合征舌苔脱落细胞调控蛋白与肝郁病理的相关性,为临床诊疗提供实验依据.本研究采用随机数字表法,选取50例健康妇女作为对照组,150例围绝经期综合征患者作为观察组,证素辨证计算肝郁积分,巴氏染色检测舌苔脱落细胞的成熟指数(MI)和成熟价值(MV),流式细胞仪检测舌苔脱落细胞凋亡指数,免疫组化检测舌苔脱落细胞调控蛋白.结果显示,围绝经期综合征肝郁积分明显高于健康妇女:肝郁病理改变,与舌苔脱落细胞MI的中层细胞数量呈正相关,与舌苔脱落细胞MI的表层细胞数量及MV呈负相关:肝郁病理改变,与舌苔脱落细胞凋亡指数、Fas、Bax的阳性率呈正相关,与舌苔脱落细胞中Bcl-2的阳性率呈负相关.提示肝郁病理是围绝经期综合征的核心病机之一,肝郁病理与舌苔脱落细胞的成熟度、凋亡指数及凋亡调控蛋白相关.     

结合奇偶测试的大规模集成电路征兆测试

征兆测试是一种高效简捷的电路测试方法。该文提出一种适用于大规模集成电路的测试方法——组合征兆测试法。利用这种方法,测试者可以通过穷举输入组合,使奇偶测试和征兆测试相结合,共同解决对大规模集成电路故障测试的难题。主要思想是:首先通过被测电路的奇偶性判断该电路的征兆测试法的可测性,对征兆测试法不可测的电路,引入高阶征兆测试的思想,使其成为高阶征兆测试法可测电路。结果表明:该方法在提高可测性的同时,还提高了电路征兆测试的测试效率和故障覆盖率。通过对一些基准电路和常用电路的测试验证了该方法的实用性。     

白斑综合征病毒对日本囊对虾仔虾免疫相关酶活性的影响

用含对虾白斑综合征病毒(WSSV)的病虾组织匀浆上清液对日本囊对虾(Marsupenaeus japonicus)仔虾进行攻毒,于0,6,12,24,36,48,72,96,144 h时间点取样,以研究WSSV对仔虾体内总蛋白含量、酸性磷酸酶(ACP)、碱性磷酸酶(AKP)、超氧化物歧化酶(SOD)和酚氧化酶(PO)活性的影响.结果表明:投喂感染后,与吞噬作用相关的水解酶ACP、AKP呈显著变化,于24 h时达到最大值;与氧化应激有关的SOD和PO也变化显著,分别于72和6 h达到最高值;ACP、AKP、SOD和PO均对病原反应敏感,可以作为WSSV入侵日本囊对虾的参考指标.     

How do Shp2 mutations that oppositely influence its biochemical activity result in syndromes with overlapping symptoms?

Activating and inactivating mutations of SHP-2 are responsible, respectively, for the Noonan (NS) and the LEOPARD (LS) syndromes. Clinically, these developmental disorders overlap greatly, resulting in the apparent paradox of similar diseases caused by mutations that oppositely influence SHP-2 phosphatase activity. While the mechanisms remain unclear, recent functional analysis of SHP-2, along with the identification of other genes involved in NS and in other related syndromes (neurofibromatosis-1, Costello and cardio-facio-cutaneous syndromes), strongly suggest that Ras/MAPK represents the major signaling pathway deregulated by SHP-2 mutants. We discuss the idea that, with the exception of LS mutations that have been shown to exert a dominant negative effect, all disease-causing mutations involved in Ras/MAPK-mediated signaling, including SHP-2, might lead to enhanced MAPK activation. This suggests that a narrow range of MAPK signaling is required for appropriate development. We also discuss the possibility that LS mutations may not simply exhibit dominant negative activity. Received 30 November 2006; received after revision 8 February 2007; accepted 13 March 2007     

Chronobiology of sleep in humans

Periodic circadian (24-h) cycles play an important role in daily hormonal and behavioural rhythms. Usually our sleep/wake cycle, temperature and melatonin rhythms are internally synchronized with a stable phase relationship. When there is a desynchrony between the sleep/wake cycle and circadian rhythm, sleep disorders such as advanced and delayed sleep phase syndrome can arise as well as transient chronobiologic disturbances, for example from jet lag and shift work. Appropriately timed bright light is effective in re-timing the circadian rhythm and sleep pattern to a more desired time, ameliorating these disturbances. Other less potent retiming effects may also be obtained from the judicious use of melatonin and exercise.     

The molecular role of the Rothmund-Thomson-, RAPADILINO- and Baller-Gerold-gene product, RECQL4: recent progress

The RecQ family of DNA helicases is highly conserved throughout evolution and plays an important role in the maintenance of genomic stability in all organisms. Mutations in three of the five known family members in humans, BLM, WRN and RECQL4, give rise to disorders that are characterized by predisposition to cancer and premature aging, emphasizing the importance of studying the RecQ proteins and their cellular activities. Interestingly, three autosomal recessive disorders have been associated with mutations in the RECQL4 gene: Rothmund-Thomson, RAPADILINO, and Baller-Gerold syndromes, thus making RECQL4 unique within the RecQ family of DNA helicases. To date, however, the molecular function of RECQL4 and the possible cellular pathways in which it is involved remain poorly understood. Here, we present an overview of recent findings in connection with RECQL4 and try to highlight different directions the field could head, helping to clarify the role of RECQL4 in preventing tumorigenesis and maintenance of genome integrity in humans. Received 31 October 2006; received after revision 4 January 2007; accepted 5 February 2007